IgM-Rheumatoid Factor, Anti-Cyclic Citrullinated Peptide, and Anti-Citrullinated Human Fibrinogen Antibodies Decrease During Treatment with the Tumor Necrosis Factor Blocker Infliximab in Patients with Rheumatoid Arthritis

MARIJN VIS, WOUTER H. BOS, GERTJAN WOLBINK, ALEXANDRE E. VOSKUYL, JOS W.R. TWISK, ROB van de STADT, DÖRTE HAMANN, BEN A.C. DIJKMANS, and WILLEM F. LEMS

ABSTRACT.

Objective. To investigate the effect of treatment with infliximab on serum levels of rheumatoid factor (IgM-RF), antibodies against cyclic citrullinated peptide (anti-CCP), and antibodies against deiminated human fibrinogen, a specific citrullinated peptide (ACF), and their association with disease activity and disease duration in patients with rheumatoid arthritis (RA).

Methods. The study sample included 62 consecutive patients who were treated with infliximab for at least one year. IgM-RF, anti-CCP, and ACF were measured at 0, 14, 30, and 46 weeks.

Results. Patients had a mean age of 54 years and median disease duration of 10 years and were predominantly female (81%). At baseline 63%, 77%, and 82% of patients were positive for IgM-RF, anti-CCP, and ACF, respectively. In terms of percentages, the levels of IgM-RF were reduced by 64% at 46 weeks, while anti-CCP and ACF levels were reduced by roughly 25%. The decrease in serum levels of these autoantibodies was not associated with the decrease in disease activity. The change in ACF was significantly related to disease duration, while the changes in IgM-RF or anti-CCP were not.

Conclusion. In a cohort of patients with RA who responded to infliximab therapy, all autoantibodies decreased significantly, but IgM-RF showed a larger decrease than anti-CCP or ACF. These changes in levels of autoantibodies are not directly related to the change in disease activity. Early in the disease, ACF levels were best influenced by treatment with infliximab. (J Rheumatol 2008; 35:425-8)

Key Indexing Terms:

RHEUMATOID ARTHRITIS
RHEUMATOID FACTOR
ANTI-CYCLIC CITRULLINATED PEPTIDE
INFLIXIMAB

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From VU University Medical Center, Sanquin Research, and Jan van Breemen Institute, Amsterdam, The Netherlands.

M. Vis, MD; A.E. Voskuyl, MD, PhD; J.W.R. Twisk, PhD, VU University Medical Center; D. Hamann, PhD, Sanquin Research; R. van de Stadt, PhD, Jan van Breemen Institute; W.H. Bos, MD; G. Wolbink, MD, PhD, Sanquin Research and Jan van Breemen Institute; B.A.C. Dijkmans, MD, PhD; W.F. Lems, MD, PhD, VU University Medical Center and Jan van Breemen Institute.

Address reprint requests to Dr. M. Vis, VU University Medical Center, Department of Rheumatology, 4A42, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. E-mail: m.vis@vumc.nl

Accepted for publication September 17, 2007.

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